A GABA A MEDIATED AFTERDEPOLARIZATION IN PYRAMIDAL NEURONS FROM RAT
NEOCORTEX.
Cerne, R. and W. J. Spain.
Veterans Affairs Puget Sound Health Care System, Seattle, WA 98108 and the
Departments of Neurology and Physiology & Biophysics, University of Washington
School of Medicine, Seattle, WA 98195.APStracts 3:0244N, 1996.
ABSTRACT
We report a novel slow afterdepolarization (sADP) in layer V pyramidal neurons
when brain slices from somatosensory cortex are perfused with GABA. Whole-cell
recordings were made from visually-identified neurons in slices from 3 to 5
week old rats. The firing of action potentials at 100 Hz for 1 second, evoked
by a train of brief current pulses, is typically followed by a slow
afterhyperpolarization (sAHP). When GABA (1 mM) was applied to the perfusate,
the sAHP was replaced by a sADP of nearly equal to 18 mV in amplitude, which
on average lasted for 26 seconds. The sADP was not evoked or terminated as an
all-or-none event: it grew in amplitude and duration as the number of evoked
action potentials was increased; and when the sADP was interrupted with
hyperpolarizing current steps, its amplitude and duration were graded in a
time and voltage dependent manner. The sADP did not depend on Ca 2+ entry into
the cell: it could be evoked when bath Ca 2+ was replaced by Mn 2+ or in
neurons dialyzed with 20 mM BAPTA. We hypothesized that the sADP was
predominantly generated in the dendrites because it was associated with the
firing of small-amplitude action potentials which continued after the somatic
membrane potential was repolarized to -70 mV by steady current injection. We
tested this hypothesis by evoking the sADP in neurons with surgically
amputated apical dendrites. In those neurons the average duration of the sADP
was 78% shorter then in neurons with an intact apical dendrite and there were
no associated small action potentials. The sADP was also evoked by muscimol,
but not by baclofen, and was blocked by bicuculline or picrotoxin but not by
CGP 35348 indicating that it is mediated through the activation of GABA A
receptors. Our results suggest that intense activity in the presence of GABA
results in a long lasting enhancement of excitability in the apical dendrite
which could in turn lead to amplification of distal excitatory synaptic
potentials.

Received 17 October 1996; accepted in final form 21 October 1996.
APS Manuscript Number J528-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996